Decreased production of MCP-1 and MMP-2 by keloid-derived fibroblasts.
Keloid tissue results from aberrant wound healing. The underlying mechanism responsible for keloid formation remains unclear. The aim of this study was to analyse the production of tissue inflammatory mediators by normal and keloid-derived human dermal fibroblasts cultured in vitro. Production of monocyte chemoattractant protein 1 (MCP-1), matrix metalloproteinase 2 (MMP-2) and tissue inhibitor of metalloproteinase 2 (TIMP-2), with and without the addition of interleukin-1beta, was determined by enzyme-linked immunosorbant assay. Our results showed that IL-1beta (10 ng/ml) stimulated a statistically significant increase in MCP-1 and MMP-2 production and decreased production of TIMP-2 by both normal and keloid-derived fibroblasts (Student's t-test, p<0.05), but to differing extents. This may contribute to factors leading to keloid formation.
Yeh
Fa-Lai
FL
Department of Surgery, Division of Plastic and Reconstructive Surgery, Taipei Veterans General Hospital and National Yang-Ming University, Taipei, Taiwan, ROC. flyeh@vghtpe.gov.tw
Shen
Horng-Der
HD
Tai
Hsiao-Yun
HY
D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis*; D004797:Enzyme-Linked Immunosorbent Assay; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D053583:Interleukin-1beta / Q000494:pharmacology*; D007627:Keloid / Q000378:metabolism*; D020778:Matrix Metalloproteinase 2 / Q000096:biosynthesis*; D012867:Skin / Q000378:metabolism; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000096:biosynthesis; D014945:Wound Healing / Q000502:physiology
D018932:Chemokine CCL2; D053583:Interleukin-1beta; D019716:Tissue Inhibitor of Metalloproteinase-2; D020778:Matrix Metalloproteinase 2